Micro-injection of propranolol within basolateral amygdala impaired fear and spatial memory and dysregulated evoked responses of CA1 neurons following foot shock stress in rats.

Abstract The basolateral nucleus of the amygdala (BLA) is responsible for memory retrieval after stress. It regulates hippocampal long-term potentiation (LTP) during stress. Although β-adrenoceptors of the BLA have a critical role in memory, few studies have addressed this question in the BLA, and the results still have been contradictory. The present study was designed to investigate the involvement of β-adrenoceptors of the BLA on hippocampus memory, anxiety, and plasticity in intact and stressed rats. Male Wistar rats were submitted to the electrical foot-shock stress for four consecutive days. Over four consecutive days, animals received bilateral micro-injections of either vehicle or propranolol (4 µg in 1 µl/side) into the BLA (5 min before foot-shock stress). Behavioral (memory, as well as anxiety-like behaviors), electrophysiological, and histological (neural arborization in the hippocampal CA1 pyramidal neurons) studies were performed. Results showed that inhibition of β-adrenoceptors of BLA by propranolol significantly further impaired fear and spatial memory in stressed rats. Similarly, propranolol effectively impaired both memories in the intact animals. Propranolol significantly amplified the slope and amplitude of fEPSP in the CA1 area of the hippocampus only in stressed rats. Foot-shock stress significantly increased the number of dendritic branches in the hippocampus, and propranolol suppressed this effect of stress. It is suggested that β-adrenoceptors in the BLA promote memory and reduce anxiety-like behaviors under tonic and stress conditions. Propranolol dysregulated LTP parameters and reduced dendritic branches, resulting in memory impairment. Probably β-adrenoceptors of BLA regulate evoked responses of CA1 neurons only in stress- and not the tonic condition.